NKp44 Lentiviral Activation Particles (h): sc-407295-LAC

Human NCR2 encodes NKp44 (CD336), an activating receptor selectively expressed on activated natural killer (NK) cells that recognizes diverse ligands on stressed, infected, or transformed cells. Upon engagement, NKp44 signals through the ITAM-bearing adaptor DAP12 (TYROBP), promoting Syk/ZAP70-dependent cascades that couple to MAPK and NF-κB programs to regulate degranulation and cytokine production. NCR2/NKp44 activity shapes innate immune surveillance at mucosal and tumor interfaces and is frequently interrogated in studies of inflammation, infection, and cancer immunobiology. Dysregulated NKp44 signaling and ligand availability have been associated with altered NK-cell effector function in multiple disease contexts, supporting its use as a mechanistic marker of NK activation states.

NKp44 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient NCR2 upregulation across a broader range of human cell types.

NKp44 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the NCR2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous NKp44 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NCR2 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.